1998
DOI: 10.1006/jmbi.1998.2206
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Human immunodeficiency virus type 1 vpr protein transactivation function: mechanism and identification of domains involved

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Cited by 64 publications
(52 citation statements)
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“…In addition, Vpr has been shown to interact with the viral protein, R interacting protein 1 (Rip-1), and both Rip-1 and Vpr can be co-immunoprecipitated with GR as part of the activated receptor complex (Refaeli et al 1995). Vpr action as a GR cofactor requires an intact GRE and is dependent on the ligand and the presence of the receptor, but is independent of cell-cycle arrest (Sherman et al 2000), as has been suggested by others (Forget et al 1998). In addition, GR affinity can vary in patients with AIDS, with some expressing normal affinity GR and others low-affinity receptors (Norbiato et al 1997).…”
Section: Effect Of Viral Proteins On Grmentioning
confidence: 66%
“…In addition, Vpr has been shown to interact with the viral protein, R interacting protein 1 (Rip-1), and both Rip-1 and Vpr can be co-immunoprecipitated with GR as part of the activated receptor complex (Refaeli et al 1995). Vpr action as a GR cofactor requires an intact GRE and is dependent on the ligand and the presence of the receptor, but is independent of cell-cycle arrest (Sherman et al 2000), as has been suggested by others (Forget et al 1998). In addition, GR affinity can vary in patients with AIDS, with some expressing normal affinity GR and others low-affinity receptors (Norbiato et al 1997).…”
Section: Effect Of Viral Proteins On Grmentioning
confidence: 66%
“…Moreover, the absolute levels of nuclear-associated viral cDNA were approximately sevenfold higher with the wt virus than with the cPPT-defective virus. The integrity of the fractionation procedure was validated by detection of mitochondrial DNA and ␤-globin DNA, as described previously (18,36,38). Results showed that mitochondrial and ␤-globin DNAs were found solely in the cytoplasm and the nucleus, respectively (Fig.…”
mentioning
confidence: 86%
“…In contrast, this protein does not appear to confer a significant viral growth advantage in primary T cells (11,12). However, recent studies provided evidence that vpr up-regulates HIV-1 replication during infection of dividing T cells as a result of its capacity of modulating the cell cycle progression (13)(14)(15). In this regard, it has been demonstrated that vpr expression can induce cell cycle arrest in the G 2 /M phase (13, 14, 16 -22).…”
mentioning
confidence: 99%